In fetal sheep, adaptation to chronic anemia includes a 30% increase in heart to body weight ratio, a 50% increase in stroke volume and cardiac output, a six-fold increase in coronary blood flow, and a doubling of coronary conductance with preservation of coronary reserve. Remarkably, while resting coronary flow is normal in adult sheep that were anemic in-utero, adult coronary conductance remains high, even if the anemia is corrected prior to birth. During acute hypoxia, adult sheep that were anemic in-utero but transfused prior to birth increase their indices of left ventricular systolic function, whereas controls do not. These findings suggest that the coronary vascular tree can be altered by in-utero events and that these changes may persist into adulthood. Furthermore, these changes may represent a positive aspect of fetal programming. The broad goal of the proposed studies is to determine the functional significance of alterations in the coronary vascular tree that occur secondary to fetal anemia. In this application we propose to continue our investigation of the functional effects of in-utero anemia upon the adult heart. We propose to address three major questions: First, does the increase in maximal coronary conductance represent a structural or functional modification in the adult coronary arterial tree. Second, does the increase in coronary conductance confer myocardial protection by reducing infarct size following coronary occlusion and is this protection mediated by lymphatic flow. Third, does an increase in coronary conductance result in an advantage to the adult myocardium as it develops left ventricular hypertrophy in response to systolic load? We ask these questions knowing that there is a general paucity of data regarding the effects of fetal coronary vascular growth upon adult cardiac function.